Human Adipose Tissue Lipoprotein Lipase: Comparison of Assay Methods and Expressions of Activity

Pykälistö, Olavi; Smith, Phillip H.; Brunzell, John D.

doi:10.3181/00379727-148-38526

Cited by 21 publications

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“…Since the number of fat cells appears to be normal in adult onset obesity (52,53), the expression of LPL activity per cell may provide a quantitative evaluation of the plasma TG removal system of adipose tissue in adults with varying degrees of obesity (36). If so, the plasma TG removal capacity, as related to adipose tissue, would appear to be increased in obesity.…”

Section: Methodsmentioning

confidence: 99%

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Determinants of human adipose tissue lipoprotein lipase. Effect of diabetes and obesity on basal- and diet-induced activity.

Pykälistö¹,

Smith²,

Brunzell³

1975

J. Clin. Invest.

280

106

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A B S T R A C T The role of insulin in the regulation of human adipose tissue lipoprotein lipase was evaluated. Adipose tissue heparin-releasable lipoprotein lipase (thought to be related to peripheral clearance of plasma triglycerides) was low in insulin-deficient, untreated hyperglycemic diabetic subjects (P <0.001) and treatment of hyperglycemia returned the activity to normal. In chronic hyperinsulinism, represented by obesity, heparin-releasable activity among control subjects was correlated to percent of ideal body weight (r = 0.53, P < 0.05) and to fat cell size (r = 0.61, P < 0.02).Acetone-ether powder lipoprotein lipase activity (presumed to reflect total tissue enzyme) was also related to percent of ideal body weight (r = 0.76, P < 0.001 for controls; r = 0.67, P <0.05 for diabetics) and to fat cell size (r = 0.71, P <0.01 for controls; r = 0.85, P <0.01 for diabetics. Postprandial-stimulated insulin secretion was related to diet-induced changes in lipoprotein lipase in control subjects; both were dependent upon the amount of dietary carbohydrate. In contrast, the diabetic patients with low insulin responses, failed to increase lipoprotein lipase activity with feeding. The changes in heparin-releasable (r = 0.66, P <0.01) and acetone-ether powder (r = 0.69, P <0.01) activity during feeding were related to the percent increase in plasma insulin.Thus, insulin appears to be important in the regulation of human adipose tissue lipoprotein lipase activity. Elevated insulin levels in obesity and increased insulin secretion after eating were associated with increased lipoprotein lipase activity. Defects in insulin secretion, both in postabsorptive and postprandial states, are asThis study represents a part of the clinical investigation by the late Dr. Olavi J. Pykdlist6 during a fellowship at the Veterans Administration Hospital in Seattle, Wash.

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Section: Methodsmentioning

confidence: 99%

“…The enzyme activities of the incubation medium and the acetone powder extract were assayed as previously described using triolein emulsified with lecithin as the substrate (36). Strict adherence to the procedure of sonication of the substrate minimized day-to-day variability in substrate.…”

Section: Methodsmentioning

confidence: 99%

Determinants of human adipose tissue lipoprotein lipase. Effect of diabetes and obesity on basal- and diet-induced activity.

Pykälistö¹,

Smith²,

Brunzell³

1975

J. Clin. Invest.

280

106

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show abstract

“…16,17 AT-LPL activity and lipolysis assay Heparin-releasable LPL activity was measured as previously described. 18 AT-LPL activity was expressed as nmol of FFA produced per gram of tissue in 1 min. Glycerol released from adipose cells was used as the index of lipolysis, since it is not re-utilized by the adipose cell.…”

Section: Adipose Cell Metabolismmentioning

confidence: 99%

Weight gain and adipose tissue metabolism after smoking cessation in women

et al. 2001

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BACKGROUND: Cigarette smoking increases the risk of cardiovascular disease, and is an important preventable cause of death and illness. One major deterrent to smoking cessation is a gain in body weight. Understanding the mechanisms that contribute to this weight gain may maximize the success of long-term smoking cessation. We hypothesized that smoking cessation is associated with an increase in adipose tissue lipoprotein lipase (AT-LPL) activity and=or a decrease in lipolysis, two metabolic factors that determine the balance between fat storage and fat utilization, and thus affect the propensity for weight gain. MATERIALS AND METHODS: Ten premenopausal women (37.1 AE 6.2 y, 31.7 AE 6.4 kg=m 2 body mass index (BMI), mean AE s.d.) participated in a 4 week smoking cessation program. Measurements of body weight, waist and hip circumferences, adipose cell metabolism and resting metabolic rate were obtained at baseline and after 4 weeks of smoking cessation. RESULTS: Of the 10 women who began the intervention, five successfully completed the smoking cessation intervention. After 4 weeks of smoking cessation, there were significant increases in body weight (95.1 AE 13.9 -97.7 AE 14.4 kg, P < 0.05), with no change in waist and hip circumferences or resting energy expenditure. Gluteal AT-LPL activity significantly increased in all women by 2.8-fold (1.65 AE 1.30 -4.72 AE 3.34 nmol=g=min, P < 0.05). Abdominal AT-LPL activity increased in four out of the five women, but did not reach statistical significance (1.14 AE 0.88 -3.50 AE 3.76 nmol=g=min, P ¼ 0.14). The increase in body weight correlated with the increase in gluteal AT-LPL activity (r ¼ 0.89, P < 0.05), as well as the baseline activity of gluteal AT-LPL (r ¼ 0.86, P ¼ 0.06). There were no changes in basal or stimulated lipolysis in the gluteal or abdominal fat depots. CONCLUSIONS: These results suggest that smoking cessation is associated with significant increases in body weight, as well as changes in adipose cell metabolism, in particular increases in AT-LPL activity. This increase in LPL activity may contribute to the increase in body weight associated with smoking cessation.

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“…Maternal surface cotyledons were Placenta or adipose tissue pieces were incubated in KRP medium containing 2 units/ml heparin for 45 min at 37 °C and then 1 -ml aliquots incubated with 0.2 ml artifical l -l4C triolein substrate to assay lipolytic activity [43]. Prolamine or NaCl were added to the assay mixture in the amounts or molarities indicated (sec text for details).…”

Section: Placental Lipoprotein Lipase Activity and The Effect Of Diabmentioning

confidence: 99%

Lipoprotein Metabolism in Pregnancy, Fat Transport to the Fetus, and the Effects of Diabetes

et al. 1986

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The objective of this paper is to review the extent and mechanisms of lipoprotein alterations in pregnancy, present new data relating to placental lipid transport in. normal humans and diabetic animals and consider possible effects on fetal growth and development in normal and diabetic pregnancy. The concentration of all lipoprotein fractions increases during pregnancy. VLDL cholesterol and triglyceride increase 2.5-fold over prepregnancy levels and LDL cholesterol increases 1.6-fold, all with peak levels at term. HDL cholesterol is maximally increased in midgestation by 1.45-fold and subsequently declines to 1.15-fold at term. The mechanisms of these lipoprotein changes have not been studied in humans but the hypertriglyceridemia in animal models is related to enhanced VLDL entry into the circulation. In addition, diminished adipose tissue lipoprotein lipase (LPL) activity in late gestation may cause a rerouting of triglyceride fatty acids to other tissues such as muscle and uterus for oxidation, rather than storage, since triglyceride transport is not reduced in pregnancy. All of these changes appear to be sex hormone mediated. In diabetic pregnancies, the available data indicate that triglyceride concentrations are increased and HDL cholesterol concentrations are decreased with reference to lipoproteins in nondiabetic pregnant women. Previously unpublished data show that a transplacental FFA gradient exists across the umbilical circulation in the direction of the fetus and is proportional to the maternal FFA concentration. No gradient is seen for triglyceride or total plasma cholesterol. However, transport of unmeasured amounts of triglyceride fatty acids may still occur via placental LPL and be exaggerated in diabetes where LPL declines in adipose tissue but not in placenta. The mechanism of transplacental cholesterol transport remains to be defined. Preliminary studies suggest that it depends on HDL as well as LDL since both can provide cholesterol for placental progesterone synthesis. In addition, fetal weight and length are associated with maternal apoproteins A-I and A-II, both major apoproteins of HDL. By lowering HDL in pregnancy, diabetes mellitus could negatively affect these relationships. In conclusion, sex hormone mediated modifications of lipoprotein physiology are described in pregnancy which may enhance triglyceride fatty acid transport to muscle for oxidation and LDL and HDL cholesterol delivery to growing maternal and fetal tissues, a process that diabetes could globally disrupt.

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Human Adipose Tissue Lipoprotein Lipase: Comparison of Assay Methods and Expressions of Activity

Cited by 21 publications

References 0 publications

Determinants of human adipose tissue lipoprotein lipase. Effect of diabetes and obesity on basal- and diet-induced activity.

Determinants of human adipose tissue lipoprotein lipase. Effect of diabetes and obesity on basal- and diet-induced activity.

Weight gain and adipose tissue metabolism after smoking cessation in women

Lipoprotein Metabolism in Pregnancy, Fat Transport to the Fetus, and the Effects of Diabetes

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